Gastrointestinal Metabolism of Cadmium in Experimental Iron Deficiency;

The average gastrointestinal uptake 4 h after an intragastric dose of 400 nmol of cadmium chloride labeled with 109CdCl2 in iron-deficient mice, 25%, was significantly greater than the result, 16%, in iron-normal animals, and more cadmium entered the body of the former, 3.8%, than the latter, 2% (P less than 0.05). Between 4 and 72 h, gastrointestinal radioactivity declined without further increase in body activity; however, more radiocadmium remained in the duodenum of iron-deficient than iron-normal animals (P less than 0.05). The radiocadmium sequestered in the duodenum was bound to a protein with a molecular weight of about 12,000. After subcutaneous injection of radiocadmium, the rate of excretion of radioactivity from the body was similar in iron-normal and iron-deficient mice; however, a greater proportion of the injected dose accumulated in the duodenum of the iron-deficient animals (P less than 0.05). Thus, the intestinal adapative response to iron deficiency may enhance cadmium toxicity, whereas sequestration and subsequent excretion of cadmium by the intestinal mucosa serves to protect the body against toxic effects. The duodenum, particularly in iron-deficient mice, is especially vulnerable to the toxic effects of cadmium.